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ORIGINAL ARTICLE
Year : 2022  |  Volume : 25  |  Issue : 3  |  Page : 315-324

Gastric intestinal metaplasia: Long-term follow-up results


1 Department of Gastroenterology, Recep Tayyip Erdogan University, Rize, Turkey
2 Department of İnternal Medicine, Recep Tayyip Erdogan University, Rize, Turkey
3 Department of Anesthesiology, Bilim University, Istanbul, Turkey
4 Department of Pathology, Recep Tayyip Erdogan University, Rize, Turkey

Date of Submission25-May-2021
Date of Acceptance30-Dec-2021
Date of Web Publication16-Mar-2022

Correspondence Address:
Dr. H Rakici
Department of Gastroenterology, Recep Tayyip Erdogan (RTE) University, Islampasa mah, Rize - 53100
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/njcp.njcp_1548_21

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   Abstract 


Baackground: Precancerous lesions are the most commonly cited factor in gastric cancer etiology. The sequence of events in intestinal-type gastric carcinogenesis is considered to be chronic gastritis, atrophy, intestinal metaplasia (IM), dysplasia, and carcinoma, respectively. Early diagnosis and treatment of advanced precursor lesions and gastric cancer is possible by identifying and monitoring patients with such premalignant lesions. Aim: In our study, we aimed to evaluate the long-term follow-up results of intestinal metaplasia in our hospital and the rate of progression to malignancy by comparing these patients with patients who have undergone gastroscopy without a diagnosis of intestinal metaplasia. Material and Method: One hundred and fifty-six followed-up patients out of 700 between the ages of 18 and 85 who were admitted to our hospital between 2009 and 2019, who were diagnosed with IM by pathological examination from biopsy material, and 150 patients who were not diagnosed with IM between 2009 and 2011 were included. The results of the cases were evaluated first retrospectively; then, the patients who were invited for control and underwent endoscopy were evaluated prospectively. IM and control groups were compared in terms of dysplasia and gastric cancer development. In addition, the IM group was compared in terms of 5 and 10 years of follow-up, extensive or local involvement, and complete and incomplete involvement in terms of dysplasia and cancer development. Results: The follow-up period of the patients ranged from 1 to 10 years, and the mean follow-up interval was 4.2 ± 2.8 (min: 1; max: 10) years. Age, gender, and pathology results of the patients were examined in terms of IM type, localization of IM, pathology accompanying IM, and presence of Helicobacter pylori (Hp) infection and compared with the control group. While gastric carcinoma was detected in three of 156 patients in the IM group, gastric carcinoma was not detected in the follow-up of 150 patients in the control group. IM was most common in the antrum. Incomplete IM was detected in 89 patients, and complete IM in 69 patients. While two of the three patients with gastric carcinoma were localized to the antrum, one patient had incomplete-type IM and two patients had complete-type IM, and Hp was positive in two patients. While dysplasia was detected in nine of the patients diagnosed with IM, it was detected in two patients in the control group. A statistically significant difference was found between the IM and control groups in terms of dysplasia positivity (p = 0.037). On the other hand, no statistically significant difference was found between the IM and control groups in terms of age-group, gender, follow-up time group, and Hp positivity (p > 0.05). There was no significant difference between those who were followed up for 5 and 10 years in the IM group in terms of dysplasia and cancer development. Conclusion: Therefore, it is considered that patients with intestinal metaplasia may be followed up at longer intervals, except for patients with race, ethnicity, incomplete type, extensive involvement, and a family history of gastric cancer.

Keywords: Dysplasia, follow-up, gastric cancer, intestinal metaplasia


How to cite this article:
Rakici H, Uyanik E, Rakici I M, Polat H B, Akdogan R A, Aydin G, Ayvaz M A, Bedir R. Gastric intestinal metaplasia: Long-term follow-up results. Niger J Clin Pract 2022;25:315-24

How to cite this URL:
Rakici H, Uyanik E, Rakici I M, Polat H B, Akdogan R A, Aydin G, Ayvaz M A, Bedir R. Gastric intestinal metaplasia: Long-term follow-up results. Niger J Clin Pract [serial online] 2022 [cited 2022 Aug 19];25:315-24. Available from: https://www.njcponline.com/text.asp?2022/25/3/315/339715




   Introduction Top


Although gastric cancers are the fifth most common cancer worldwide, they rank third among cancers that cause death.[1] Since early-stage gastric cancers are generally asymptomatic and their symptoms are vague, the diagnosis is usually made in the late period. Therefore, curative treatment options remain limited.[2] Premalignant lesions are known as an important risk factor for gastric cancer development.  Helicobacter pylori Scientific Name Search uses chronic inflammation of the gastric mucosa and progresses through premalignant stages such as atrophic gastritis, intestinal metaplasia (IM), and dysplasia, which lead to gastric adenocarcinomas. This carcinogenesis model is known as the multi-step gastric carcinogenesis cascade of Correa. Since the publications on the monitoring, onset, and time interval protocols of these premalignant lesions are limited, most of the available publications are retrospective and on a small number of groups.

By identifying and monitoring patients with such premalignant lesions, early diagnosis and treatment of advanced precursor lesions and gastric cancers will be possible. The progression rates of gastric cancer development from atrophic gastritis vary from 0% to 2% annually. However, progression rates of gastric cancer development from intestinal metaplasia and dysplasia range from 0% to 10% and from 0% to 73%, respectively.[4] In Japan, where screening and follow-up studies are carried out, the rate of early diagnosis is over 50% and the five-year survival in these cases is 90%. On the other hand, in countries where screening and follow-up studies are not performed, such as UK, the five-year life expectancy of patients diagnosed with gastric cancer is below 5%.[5]

Gastric adenocarcinomas are divided into four groups macroscopically as ulcerative (75%), polypoid (10%), squamous (10%), and superficial (5%).[6] Gastric cancer is histologically divided into two groups according to Lauren classification: intestinal type (well differentiated) and diffuse type (undifferentiated).[6],[7]

The normal gastric epithelium is replaced by a columnar epithelium similar to that of the small intestine and colon. This pathology is called intestinal metaplasia which can be in sparse foci or spread to large areas. It is known as a preneoplastic lesion of the stomach and is most commonly seen in the antrum.[8] In 1979, Jass and Filipe classified intestinal metaplasia as three stages using morphology and classical mucin dyes (periodic acid–Schiff, Alcian blue, and high-iron diamine).[9]

Type 1 IM: Paneth cells, goblet cells secreting sialomucin, and enterocytes with a brushy edge are seen in this type, also known as small bowel type or complete IM. It is the most common form of IM and mostly accompanied by benign lesions such as ulcers and chronic gastritis.

Type 2 IM: It is known as colonic type or incomplete IM. It is typical to observe columnar epithelium showing different degrees of differentiation. Also, goblet cells secreting neutral and acid sialomucin can be observed in this type of IM, which is deficient in absorptive cells.

Type 3 IM: It is characterized by the acid sulfomycin secreted from intermediate cells and is the most common type of IM detected in the surrounding gastric tissue in the presence of malignancy.[10]

The updated Sydney system is a comprehensive endoscopic and histological sampling protocol used for the diagnosis of intestinal metaplasia. According to this protocol, the biopsy locations in the stomach are standardized. Five biopsies are recommended: two biopsy material in the antrum, one biopsy from the incisura, one biopsy from the small curvature, and one biopsy from the greater curvature.[10] In recent years, it has been shown that the secretion of mucin core proteins (MUC) varies according to the types of intestinal metaplasia. Although MUC2 secretion is observed spontaneously in all types of intestinal metaplasia, secretion of MUC1, MUC5, and MUC6 decreases in complete intestinal metaplasia, while the amount of secretion does not change in incomplete intestinal metaplasia.[11],[12] In the future, MUC determination in patients with intestinal metaplasia is expected to be more significant in terms of cancer risk determination. The fact that intestinal metaplasia involves the antrum and the corpus at the same time is called extensive involvement and is considered to be associated with an increased risk of malignancy. This risk increases in the presence of ethnic origin and a family history of gastric cancer. In recent years, areas of intestinal metaplasia have been detected better with magnified or non-magnified chromoendoscopic methods and biopsy is taken from suspicious areas. This method replaces the gastric mapping method.

In this study, patients with intestinal metaplasia and a control group who underwent endoscopy for any reason and did not have intestinal metaplasia were compared in terms of dysplasia and gastric cancer development during the long-term follow-up. In addition, we aimed to evaluate the factors affecting the progression to gastric cancer, the rate of progression to gastric cancer, and the monitoring programs of patients with intestinal metaplasia.


   Material and Method Top


In our tertiary care hospital (Recep Tayyip Erdogan University Gastroenterology Clinic), our first group consists of 156 patients out of 700 who were admitted between 2009 and 2019 and had a pathological diagnosis of intestinal metaplasia between the ages of 18 and 85 and who were followed up for at least 1 year in biopsy material taken by gastroscopy. Disease control group includes 150 patients whose first endoscopies were performed between 2009 and 2011 and followed up for 5–10 years and were not diagnosed with IM. Both groups are included in the study retrospectively.

In 2018 and 2019, endoscopy was performed on patients who are not monitored from both groups. In this sense, the study has continued prospectively. Recep Tayyip Erdogan University Faculty of Medicine ethics committee approval was obtained. At least five biopsies were taken from patients who were found to have intestinal metaplasia and underwent control endoscopy, and their follow-up was continued. Patients with intestinal metaplasia were followed up by taking biopsy from irregular areas with narrow band imaging (NBI) images in control endoscopies.

Pathological examination was conducted by different pathologists. Intestinal metaplasia and control groups were compared in terms of dysplasia and cancer development. In addition, we aimed to evaluate the factors affecting the progression of gastric cancer in patients with intestinal metaplasia, the rate of progression to gastric cancer, and the follow-up programs of patients with intestinal metaplasia. Five- and 10-year follow-ups were compared in terms of dysplasia and adenocarcinoma development in the group with IM. In this respect, wide (both antrum and corpus) and local involvements (only antrum) and complete and incomplete involvements were compared. Patients who underwent gastric and esophageal surgery and those with previously known gastric malignancies were excluded from the study.

The research data were uploaded to the computer environment via “SPSS (Statistical Package for Social Sciences) for Windows 22.0 (SPSS Inc., Chicago, IL)” and evaluated. Descriptive statistics were presented as mean ± standard deviation (minimum–maximum), frequency distribution, and percentage. Pearson's Chi-square test and Fisher's exact test were used to evaluate categorical variables. The suitability of the variables to normal distribution was examined using visual (histogram and probability graphs) and analytical methods (Kolmogorov–Smirnov test/Shapiro–Wilk test). The Mann–Whitney U test was used as a statistical method for the statistical significance between two independent groups, and the Kruskal–Wallis test between three or more independent groups for variables that were found to be non-compliant with the normal distribution. When a significant difference was detected between three or more independent groups, Bonferroni correction was applied in post hoc paired comparisons for the source of the difference. Statistical significance level was accepted as P > 0.05.


   Results Top


Within the scope of the study, 156 patients who were diagnosed with intestinal metaplasia (IM) by gastroscopy and followed up for at least 1 year and 150 patients who were followed up for 5–10 years and were not diagnosed with intestinal metaplasia were studied. The average age of patients diagnosed with IM was 49.5 ± 13.0 (min: 18; max: 81) years, 34.6% were under the age of 50, 43.6% were between 50 and 64 years, and 21.8% were 65 years and over. 55.8% of the patients were women. The mean follow-up period of patients with IM diagnosis was 4.2 ± 2.8 (min: 1; max: 10) years. 77.6% was localized in the antrum, while 22.4% in both antrum and corpus. It was seen that 51.9% of them were Hp negative and 48.1% were Hp positive.

A statistically significant difference was found between the genders of the patients in terms of age and age-group (p < 0.001 for both). The average age of male patients was significantly higher than that of women. In addition, the percentage of patients aged 65 years and over was significantly higher among male patients than women. The distribution of some descriptive and clinical characteristics of patients with IM and the control group is presented in [Table 1].
Table 1: Distribution of some descriptive and clinical features between IM and control groups

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On the other hand, no statistically significant difference was found between localization sites in terms of age, age-groups, gender, follow-up time, IM type, Hp status, dysplasia, and cancer development (p > 0.05). No statistically significant difference was found between the IM types (complete or incomplete) of patients in terms of dysplasia and cancer development (p > 0.05) [Table 2].
Table 2: Basic characteristics of patients with IM according to IM type and localization

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There was no statistically significant difference in terms of dysplasia and cancer development between patients with IM diagnosed with follow-up for up to 5 years and those with a 10-year follow-up [Table 3].
Table 3: Basic characteristics of patients with IM according to their follow-up period

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Gastric cancer was observed in three patients (1.9%) within the scope of the study. The mean age of these patients was 63.0 ± 10.0 (53–73) years, while their ages were 53, 63, and 73, respectively. Two of these three patients were female (66.7%), and one (33.3%) was male. The mean follow-up period was 3.7 ± 3.0 (min: 1; max: 7), and the follow-up periods were 1 year, 3 years, and 7 years, respectively. Two (66.7%) of the three patients developed adenocarcinoma, and one (33.3%) signet ring cell carcinoma. Likewise, one of the three patients (66.7%) was localized in the antrum, while two (33.3%) were localized in the corpus. The control group had similar demographic characteristics with the IM group. No cancer development was observed in the control group at 5 and 10 years of follow-up. These values were not statistically significant due to the small number of cases. In terms of the development of dysplasia, nine (5.8%) patients in the IM group and two (1.3%) patients in the control group were detected. The difference was statistically significant (p = 0.037). Dysplasia developed in the IM group in third, fourth and seventh years [Table 2]. In the control group, dysplasia was seen in the fourth and fifth years. The ethnic composition of the patients was homogeneous.


   Discussion Top


Gastric cancer is still a major health problem worldwide. It ranks fifth for incidence and third for cancer-related mortality in the most recently published global cancer statistics.[1] Intestinal metaplasia (IM) is considered to be a precancerous lesion that causes gastric cancer. It has been shown that the rate of gastric cancer development increases in patients with IM approximately six times.[13],[14] In some studies, it has been stated that the mortality rate can be decreased by diagnosing gastric cancer at an early stage by performing histological and pathological follow-up by endoscopy in patients with IM.[14] However, nowadays, guidelines prepared for endoscopic follow-up of these patients cannot fully meet the needs.

In this study, we compared the long-term follow-up results of patients with intestinal metaplasia, the factors leading to the progression of gastric cancer, and the progression to gastric malignancy in patients who were followed up with endoscopy for many years but were not diagnosed with intestinal metaplasia. According to the latest data published by European gastroenterology associations, the incidence of gastric cancer was found to be 0.1–0.25% in patients with chronic atrophic gastritis and 0.25% in patients with IM. However, having a first-degree relative with gastric cancer is a risk factor for gastric cancer. It has also been shown to have an increasing rate of between two and ten times depending on geographical region and ethnicity.[15] According to a study in the Netherlands, the annual incidence of gastric cancer for gastric intestinal metaplasia was 0.25%, 0.6% for mild-to-moderate dysplasia, and 6% for severe dysplasia, with an increase of 5.7% with a family history of gastric cancer.[14] In our study, no findings were found in the family history of patients who developed cancer and dysplasia.

Li Dan et al. described in their 10-year follow-up study, which was conducted in California, that among 4126 patients with IM and 185 patients with dysplasia, 50% of the patients with IM and 36% of the patients with dysplasia had a Helicobacter pylori (Hp) infection. Different results are observed regarding the incidence of H. pylori infection in the literature. In this study, 51.6% of the patients were female and 48.4% male and the rate of adenocarcinoma development in the patients with IM was 0.5% (20) in the first year. The incidence rate of adenocarcinoma was 0.4% after 1 year (17). While the rate of developing adenocarcinoma in the first year of patients followed up with dysplasia was 16% (31), it was determined that the rate of adenocarcinoma development after 1 year was 4% (8).[16] In the same study, they showed that the Hispanic race had the highest rate of gastric adenocarcinoma among all race/ethnic groups, although premalignant lesions were detected more in Asian race.

Since there were few African-Americans who developed gastric adenocarcinoma in this study, the risk of African-Americans was not well estimated. Also, these ethnic groups are not represented quantitatively in our country, so we could not have included them into our study.[16] In our study, 55.8% of the patients were female and 44.2% male. Adenocarcinoma developed in three patients (1.9%) within the scope of the study. Two of these three patients were female (66.7%) and one (33.3%) was male. Likewise, while two (66.7%) of the three patients were localized in the antrum, one (33.3%) had extensive involvement in the antrum and corpus. While 55.8% of the patients had incomplete IM type, the remaining 44.2% were complete. One (33.3%) of the cancer patients was complete, two (66.7%) were incomplete, two (66.7%) were Hp positive, and one (33.3%) was negative. It is reported in the literature that malignancy development is more pronounced in incomplete intestinal metaplasia. However, in our study, there was no difference between complete and incomplete.

In the 12-year endoscopy follow-up study of 573 patients with Hp positivity, 21 (3.6%) patients had progression to adenocarcinoma according to a study by Satoki Shichijo et al.[17] in Tokyo. No IM was detected in 70% of these patients, and IM was detected in 20% of the antrum and 10% of the corpus. Progression to adenocarcinoma was observed in 8 (4.5%) of 109 patients with IM in the antrum and in 7 (7.6%) of 50 patients with IM in the corpus, while only 6 (1%) of 393 patients without IM were observed to progress to adenocarcinoma. However, the conversion rate of IM in the corpus to gastric cancer was 14%, while the conversion rate of IM detected in the antrum to gastric cancer was 7%. According to this study, the cumulative incidence of gastric cancer was 0.4% at 1 year, 3.2% at 5 years, and 5.2% at 10 years.[17]

Rohit Dhingra et al.[18] observed that, in a 10-year retrospective monitoring of 1628 people, 358 patients were followed up as IM positive and Hp positivity was detected in 20% of them. Of the 358 patients, 8.9% (32) were African-American, 48% (172) Asian, 4.2% (15) Hispanic, and 38% (139) Caucasian. Eighty-seven percent (314) of the patients with IM were observed in the antrum. In this study, progression to adenocarcinoma and dysplasia in 6.6% (15) were observed in 1.7% (6) of the patients during their follow-up. In the same study, 0.07% adenocarcinoma and 1.3% dysplasia were detected in the follow-up of patients without premalignant lesions.

In our study, 77% (121) of the patients with IM were localized in the antrum, while 46.8% (75) Hp was positive. Dysplasia was present in 5.8% (9) of these patients. Progression to malignancy was detected in three (1.9%) patients; two of them developed adenocarcinoma and one with signet ring cell cancer. Adenocarcinoma was not detected in the control group of 150 people who were followed up without premalignant lesion before, and dysplasia was observed in two (1.3%) patients.

Patients with diagnosed IM had a statistically significant higher rate of dysplasia in comparison with the control group (p = 0.037), which was found to be similar to the data in the literature. The fact that no adenocarcinoma developed in the control group is important compared to the 1.9% rate of gastric cancer development in patients with IM. However, the lack of statistical significance (p = 0.24) may be due to the small sample size.

Different localizations and subtypes of IM are also different in association with cancer. According to the results of a study conducted in Portugal, it was reported that 8% of those who had complete IM in the first biopsy performed on patients and 37% of those with incomplete IM progressed to low-grade dysplasia in 3 years. In this study, no high-grade dysplasia developed in any of the patients with complete intestinal metaplasia after 3 years of follow-up. It has been shown that 15% of patients with incomplete intestinal metaplasia develop high-grade dysplasia within an average of 1 year.[19] González et al.[20] reported that the rate of conversion of incomplete IM to gastric cancer was 4–11 times higher than that of complete IM in a large multicenter study.

El-Zimaity et al.[21] reported that, during a 9-year period, incomplete IMs had their endoscopic follow-ups at 6–12-month intervals, and as a result, they did not notice any progression to dysplasia or carcinoma in any of the cases. Contrary to what is believed in this study, they stated that IM types could not be predictors of dysplasia in the future.

In our study, there was no difference between the complete and incomplete metaplasia groups in terms of the development of dysplasia.

In another study that reported that extensive involvement in IM is more important than its subtypes, Cassaro et al.[22] reported that IM, which involves the small curvature from pylorus to cardia or the whole stomach, has a higher risk of gastric cancer compared to only antrum-dominant IM.

It was first shown in epidemiological studies that there was an important link between Helicobacter pylori (Hp) infection and gastric cancers, and Hp was classified as a first group carcinogen by the International Agency for Research on Cancer in 1994. In the “Eurogast” study in which a total of 13 countries (11 European countries, Japan, and America) participated in 17 different nations, it was reported that the risk of gastric cancer is six times higher in Hp-positive patients than in Hp-negative patients.[23] With Hp infection, the risk of developing gastric cancer increases in proportion to the time, and it has been reported that the risk increases approximately nine times when the duration exceeds 15 years.[24] Hp infection is observed in prevalence ranging from 37.5% to 79.5% in our country, according to İbiş et al.[25] The prevalence of Hp was 71.2% in the study of Özdil et al.[26] They reported the prevalence of Hp as 71.3% and the frequency of metaplasia as 17.8.

According to Mete et al.'s study in Tekirdağ region, Hp was detected in 74% of patients with IM.[27] In our study, in accordance with the literature, 75 (48%) of 156 IM patients were progressing with Hp positivity. In addition, eight IM patients regressed with Hp eradication. In this context, Hp eradication is recommended to prevent the transformation of precancerous lesions into gastric cancer (especially at the stage of atrophic gastritis). In light of the available data in our study, no significant difference was found between the Hp-positive group and the Hp-negative group in terms of gastric cancer and dysplasia. Again, in the 2019 Europe (ESGE) guideline, it is reported that Hp eradication will not prevent cancer progression in patients with IM.[15]

Helicobacter pylori infection was shown to be associated with gastric cancers in epidemiologic studies, and H. pylori was determined as the first-degree carcinogen by the International Cancer Research Institute in 1994. In the “Eurogast” study with 17 participating different nations in 13 countries (11 European countries, Japan, and USA), H. pylori-positive patients had a six times higher risk of gastric cancer in contrast to H. pylori-negative patients.[23] With prevailing H. pylori infection, the risk of gastric cancer is increasingly correlating with the time of H. pylori infection as patients with a H. pylori infection period longer than 15 years have an almost nine-fold higher gastric cancer risk.[24] In our country, the prevalence of H. pylori infection differs with ranges from 37.5 to 79.5%.

Ibiş et al.[25] reported in their study a H. pylori prevalence of 71.2%, while Özdil et al.[26] detected a H. pylori prevalence of 71.3% and a rate of metaplasia of 17.8%. Mete et al. described in their study that in the region of Tekirdağ a H. pylori rate of 74% was observed among patients with H. pylori and IM.[27] According to data in the literature, we could show in our study that 75 (48%) of 156 patients with IM were H. pylori positive. Further, it was pointed out that eight patients with IM had a regression after H. pylori eradication therapy. İn this context, H. pylori eradication therapy is recommended in patients with precancerous lesions (in particular atrophic gastritis) in order to prevent transition to gastric cancer. With regard to our study, there were not identified any statistical significant differences between the H. pylori-positive and H. pylori-negative groups in relation to gastric cancer and dysplasia.

Guitark Noh et al. reported that 347 patients with a diagnosis of IM and Hp positivity were followed up with endoscopic and blood pepsinogen levels for 12–24–36 months. In their study, a decrease in PG1 level and an increase in PG1/PG2 level were found in the first 12 months after eradication. A decrease in IM activity was shown in the controls performed by the endoscopic method. This decrease was not seen in follow-up periods longer than 24 months.[10]

When patients with Hp positivity were considered, dysplasia was accompanied by 6.7% of the patients, but since the rate of dysplasia in patients with Hp-negative IM was 5.5%, a statistically significant difference was not detected in our study. In our study, in Hp-positive IM patients, IM regression was observed in eight patients after Hp eradication, seven of them were localized to the antrum, while two patients with IM regression had complete-type IM. Although IM regression of Hp therapy is still controversial, many studies have shown that Hp eradication therapy prevents the progression of atrophy and metaplasia in the gastric mucosa.[28],[29] In our study, results in this direction were obtained.

Although studies on the relationship between smoking status and intestinal metaplasia (IM), a premalignant lesion of gastric cancer, are limited, in Korea, Kyungeun Kim et al.[30] observed that the level of cotinine in urine, an objective measure of smoking, was significantly associated with an increased risk of developing IM in both men and women. For men, urine cotinine levels between 50 and 99 ng/mL, 100 and 499 ng/mL, and ≥500 ng/mL were compared, respectively, for IM 1.20, 1.26, and 1.54, while for women the ratio was 0.75, 1.86, and 1.57, respectively. Collectively, these data confirm smoking as an independent risk factor for the development of gastric IM, the precursor lesion of gastric cancer.

Those who are in the opinion of following up patients with atrophic gastritis and complete intestinal metaplasia recommend endoscopic and histological examination periods ranging from 18 to 36 months. There are opinions arguing that monitoring for this group of patients is not cost-effective and unnecessary.[31] In other studies conducted in Korea, it was reported that patients with severe IM were diagnosed more frequently with an annual endoscopic follow-up compared to every 2 years (66.7% vs. 35.5%, respectively). It has been reported that annual endoscopic follow-up is more beneficial in high-risk patients.[32] According to the latest MAPS2 guidelines published by the European gastroenterology endoscopy societies, patients with advanced stages of atrophic gastritis (both antrum and corpus), severe atrophic changes in OLGA/CASE III/IV or intestinal metaplasia) should be followed up by endoscopy every 3 years. With advanced stages of atrophic gastritis, it is recommended that patients with a family history of gastric cancer should undergo a more intensive follow-up (every year or every 2 years). When dysplasia is detected in the patient, control at 6 or 12 months is recommended.[15]

There are new methods in terms of early detection of gastric cancers and recognition of precancerous lesions. In a method called chromoendoscopy (CE), dye is applied topically to the area to be examined by means of a catheter passed through the working channel of the endoscope. It is important in terms of creating contrast that will facilitate the examination of the operating physician and to identify the lesion in its place. It is also used without magnifying. Zhao et al.[33] compared standard endoscopic method (white light endoscopy (WLE)) with CE method by evaluating 333 patients and 396 lesions. The overall accuracy of CE was 86.6%, the overall accuracy of WLE was 54.9%, and the risk difference (RD) was 0.36 (95% CI: 0.11–0.61). In another study that included 63 patients and 70 lesions specified by the review, the total accuracy of CE was 98.4%, the overall accuracy of WLE was 81.0%, and the risk difference (RD) was 0.17 (95% CI: 0.07–0.28). According to the European Society of Gastroenterology, available evidence suggests that CE-targeted biopsies and map biopsies are the best way to detect most cases of advanced gastritis, where possible, the use of CE for target biopsies.[15] In our study, index biopsies were taken using WLE and control biopsies using NBI.

The average follow-up period of patients with IM diagnosis was 4.2 ± 2.8 years, 17.3% of them were followed up for 1 year, 31.4% for 2–3 years, 23.1% for 4–5 years, and 28.2% for 6–10 years. On the other hand, no statistically significant difference was found between the patients followed for 1–5 years and those followed for 6–10 years in terms of age, age-group, gender, localization, HP status, dysplasia, and gastric cancer development. Looking at the localization, 77.6% of them were localized in the antrum and 22.4% in both antrum and corpus. While the rate of developing IM dysplasia localized to the antrum was 6.6%, it was 2.9% in the antrum plus corpus. However, there was no statistically significant difference (p > 0.05).

Dysplasia in the IM group has developed in the third, fourth, and seventh years. In the control group, dysplasia was observed in the fourth and fifth years.

In our follow-up, three patients were observed to have gastric cancer, two of them localized to antrum and one of them was focal-type IM. The mean follow-up period was 3.7 ± 3.0 (min: 1; max: 7). Malignancy detection times were in the first year, third year, and seventh year; two of the patients were women. All three patients were older than 50 years. In accordance with the literature, the progression or presence of IM increases with increasing age. There was no family history of gastric cancer in the family history of the patients who developed malignancy.

The fact that our study started retrospectively from the beginning causes the information we have to be limited to the information in the computer records. The homogeneous population structure of our society has created an obstacle for the formation of information related to race, geographical region, and ethnic group. In addition, in our study, index biopsies were taken using WLE and control biopsies using NBI. These can be considered as the limitations.


   Conclusion Top


Although its rate has decreased, gastric cancer is still an important health problem. Premalignant gastric lesions (atrophic gastritis, intestinal metaplasia, and dysplasia) are the most considered factors in the etiology of gastric cancer. These patients need to be followed up because they are at high risk of gastric cancer. In our results, dysplasia and gastric cancer development were found to be significantly higher in patients with IM compared to the control group without IM.

Although there are transitions between IM types, patients with incomplete-type IM should be followed up more frequently than patients with complete-type intestinal metaplasia. In addition, extensive involvement (both antrum and corpus attitude), family history of gastric cancer, race, and ethnicity are risk factors for the development of gastric cancer. In the current guidelines, annual follow-up is recommended for those who have these risk factors. Other than this, follow-up is recommended every 3 years. In our findings, no statistically significant difference was found regarding these risk factors. A three-year follow-up period is recommended for patients with IM without risk factors. The fact that there was no difference in terms of dysplasia and gastric cancer development between patients with IM who were followed up for 5 years and IM patients followed for 10 years in our study suggests that the recommendation of longer follow-up (for example, 5 years) for patients without risk factors should be discussed.

Hp positivity is a risk factor in the progression of precancerous lesions to gastric cancer and should be treated. Regression in gastric atrophy was shown with Hp treatment. However, this effect is not clear for patients with IM and dysplasia. Gastric precancerous lesion development is not observed in all people with Hp; differences in genetic tendency and environmental factors (such as smoking, excessive salt intake, and vitamin C deficiency) in the variability of gastric cancer rates and the variable pathogenicity of Hp affect gastric pathologies.

In patients with no visible lesions on endoscopy, precancerous pathologies can be detected, and therefore five biopsies should be taken from at least two regions. In the diagnosis of gastric precancerous conditions, the use of chromoendoscopy (CE)-magnified endoscopy should be increased to guide the location of the biopsy for staging atrophic and metaplastic changes, and to help target neoplastic lesions. These methods should replace the gastric mapping method. In this way, IM detection will become more sensitive and reliable.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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  [Table 1], [Table 2], [Table 3]



 

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